OBJECTIVES: (1) We plan to confirm our preliminary work with E. coli K-12 that, with UV radiation, back mutations occur by a one-hit process, and suppressor mutations occur by a two-hit process. (2) As controls for previous mutation studies, we observed that the different DNA repair deficient strains showed different levels of spontaneous mutagenesis in the same relative manner that these repair genes controlled UV radiation mutagenesis. To examine this phenomenon in more detail, we have studied a reversion system, but now need to study some forward mutations. We will also test various growth conditions for their possible effects on the level of spontaneous mutagenesis. (3) The recB, lexA and uvrD genes appear to act additively for survival after UV irradiation, while the recF mutation acts synergistically with these mutations. We have a new mutation (radA) that sensitizes a uvrB strain. We will test if this gene functions in the recF or the recB, uvrD, lexA pathways of postreplication repair. We will also study the effect of the radA and recF genes on the UV radiation-induction of resistance to UV radiation.